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Published on: October 19, 2013
Effects of n-3 polyunsaturated fatty acids in the fetal pulmonary circulation
Ali Houeijeh1, Estelle Aubry, Hélène Coridon
1Pôle de Médecine Périnatale, Hôpital Jeanne de Flandre, CHRU de Lille, Lille, France.
Insights
n-3 polyunsaturated fatty acids in Omegaven induced significant fetal pulmonary vasodilatation. This effect was mediated by cytochrome P450 epoxygenase and potassium channels, not nitric oxide synthase.
Area of Science:
- Cardiovascular Physiology
- Neonatal Physiology
- Nutritional Science
Background:
- n-3 polyunsaturated fatty acids may improve severe respiratory failure outcomes.
- Pulmonary circulatory effects of n-3 fatty acids are not well understood.
- Relevant to persistent pulmonary hypertension in newborn infants.
Purpose of the Study:
- Investigate the effects of n-3 polyunsaturated fatty acids on fetal pulmonary circulation.
- Determine the mechanisms of n-3 fatty acid-induced pulmonary vasodilation.
Main Methods:
- Randomized, placebo-controlled laboratory investigation in 52 lamb fetuses.
- Monitored pulmonary artery pressure and blood flow using catheters and ultrasonic flow transducers.
- Administered Omegaven (n-3 enriched) or Intralipide (n-6 enriched) lipid emulsions.
Main Results:
- Omegaven increased left pulmonary blood flow by 30% and decreased pulmonary vascular resistance by 28%.
- Intralipide had no significant effect on fetal pulmonary circulation.
- Omegaven-induced vasodilation was abolished by potassium channel blockade and attenuated by cytochrome P450 epoxygenase inhibition.
Conclusions:
- Lipid emulsions enriched in n-3 polyunsaturated fatty acids induce potent fetal pulmonary vasodilation.
- This vasodilation is mediated by cytochrome P450 epoxygenase and potassium channels.
- n-3 fatty acids represent a potential therapeutic for fetal pulmonary hypertension.
Objective:
Although evidence exists that n-3 polyunsaturated fatty acids may improve the outcome in patients with severe respiratory failure, little is known regarding their pulmonary circulatory effects. This question is clinically relevant in respiratory failure associated with pulmonary hypertension, in particular in newborn infants with persistent pulmonary hypertension. The objective of this study was to investigate the effects of n-3 polyunsaturated fatty acids on the fetal pulmonary circulation.
Design:
Randomized, placebo-controlled comparative laboratory investigation.
Setting:
University research facility.
Subjects:
Fifty-two chronically prepared lamb fetuses.
Interventions:
Catheters and ultrasonic flow transducer were placed through a left thoracotomy in the lamb fetus to determine aortic, pulmonary, and left atrial pressures and left pulmonary artery blood flow.
Measurements And Main Results:
We compared the pulmonary vascular responses to 120 mins of Omegaven (lipid emulsions enriched in n-3 polyunsaturated fatty acids) or Intralipide (lipid emulsions enriched in n-6 polyunsaturated fatty acids) infusion. Then we investigated the effects of Omegaven on the pulmonary circulation after nitric oxide synthase inhibition by L-nitro-arginine, potassium channel blockade by tetraethylammonium, and cytochrome P450 epoxygenase inhibition by (methylsulfonyl)-2-(2-propynyloxy)-benzenehexanamide. Pulmonary artery and aortic pressures as well as blood gases and plasma lactate concentrations did not change during either fat emulsion infusion. Left pulmonary blood flow increased by 30% and pulmonary vascular resistance decreased by 28% during Omegaven infusion, whereas left pulmonary blood flow and pulmonary vascular resistance did not change during Intralipide infusion. This pulmonary vascular response to Omegaven was not altered by l-nitro-arginine. At the opposite, Omegaven induced pulmonary vasodilatation was abolished by tetraethylammonium and markedly attenuated by (methylsulfonyl)-2-(2-propynyloxy)-benzenehexanamide.
Conclusions:
Lipid emulsion containing n-3 polyunsaturated fatty acids may induce a potent and sustained vasodilatation in the fetal lung. This pulmonary vasodilator response is mediated through production of vasoactive mediators by cytochrome P450 epoxygenase and through activation of potassium channels.
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